Abstract: FR-PO762
A Case of Collapsing Focal Segmental Glomerulonephritis (cFSGS) After Kidney Transplant (KT): Association with SARS-CoV-2 Infection
Session Information
- Post-Transplantation and Case Reports
November 03, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Transplantation
- 2102 Transplantation: Clinical
Authors
- Kunaprayoon, Lalida, University of Virginia, Charlottesville, Virginia, United States
- Glass, William F., University of Virginia, Charlottesville, Virginia, United States
- Leeds, Joseph T., University of Virginia, Charlottesville, Virginia, United States
- Rao, Swati, University of Virginia, Charlottesville, Virginia, United States
- Kamal, Jeanne, University of Virginia, Charlottesville, Virginia, United States
Introduction
cFSGS is manifested by high grade proteinuria and rapid decline in kidney function leading to end stage kidney disease (ESKD). Viral infections including HIV, cytomegalovirus, BK and SARS-CoV-2 can trigger cFSGS in KT. High-risk APOL1 genotype in donors is linked with higher risk of cFSGS and poor allograft outcomes.
Case Description
This is the case of a 70-year-old white man with history of renal cell carcinoma requiring unilateral nephrectomy and eventually ESKD. He received a successful deceased donor KT. After 1.5 years from KT, he developed nephrotic syndrome (creatinine (Cr) 2.2 from 1.1, proteinuria 18-23 g/24h). He had mild COVID infection 2 months prior. On biopsy, glomeruli showed podocyte hyperplasia and hypertrophy consistent with cFSGS. He had diffuse glomerulitis and peritubular capillaritis (ptc) suspicious of antibody mediated rejection. C4d ptc stain was negative with no evidence of donor specific antibodies. In addition to proteinuria management with RASS blockage, SGLT2i and spironolactone, he completed 13 sessions of plasmapheresis, 2g/kg of IVIG and 2 doses of rituximab. Follow-up biopsy (5 months later) showed progressive glomerular injury (cg2), but improvement of cFSGS. Follow-up Cr is 1.5 and proteinuria is 5 g/g. The donor reported race is white, and APOL1 genotype was negative for high-risk alleles.
Discussion
This is a case of COVID-related de novo cFSGS after KT in APOL1-negative donor and recipient. It is unique as cFSGS manifested 2 months after COVID resolution. Though, case series have shown a link of APOL1 high-risk genotype with COVID19-related cFSGS, cFSGS in KT recipient from APOL1-negative donors has been reported. It is important to rule out a concomitant or recent history of rejection or viral infection in KT recipients with cFSGS. Aggressive treatment is warranted to salvage the kidney allograft.
Figure A: Light microscopy (LM)-glomerulus with variably collapsed capillaries, extracapillary hypercellularity with prominent podocyte protein reabsorption droplets & segmental glomerulitis (PASx200) Figure B: LM-glomerular capillary collapse & extracapillary hypercellularity (Silverx200)